An important structural event following myocardial infarction (MI) is LV remodeling which can be generally defined as changes within the cellular and extracellular constituents of the myocardial wall leading to changes in myocardial geometry subsequently leading to changes in LV volumes (Erlebacher J A, et al. 1984; Pfeffer M A, et al. 1990; St. John Sutton M, et al. 1994). The rate and extent of this post-MI remodeling process has been established to be independent predictors of morbidity and mortality (White H D, et al. 1987; Chareonthaitawee, P, et al. 1995). Thus, identification of those patients at the greatest risk for developing post-MI remodeling as well as identifying basic mechanisms which contribute to post-MI remodeling hold great diagnostic/therapeutic relevance. However, practicable methods for identifying patients at the greatest risk for developing post-MI remodeling have not heretofore been available.